Clearing Plaques In Blood Vessels In Alzheimer's Disease

Scientists have uncovered the role of two critical proteins that negatively affect the clearance of amyloid beta in the brain, the accumulation of which is thought to lead to the development of Alzheimer's disease. The research, published online in Nature Cell Biology this week, identifies potential therapeutic targets for treating defects associated with cognitive decline and faulty clearance of amyloid beta in brain blood vessels.

The exact causes of Alzheimer's disease are still unclear. Previous studies have shown that the disease is associated with plaques or tangles of protein fragments in the brain. These fragments, known as amyloid beta, accumulate in small arteries of the brain and contribute to the defects that occur during Alzheimer's disease.

Berislav Zlokovic and colleagues examined the effect of two interacting proteins, SRF and MYOCD, which bind to DNA and control gene expression. They show that these proteins are highly expressed in blood vessel cells in Alzheimer's patients and in mouse models of the disease, and that high levels of these proteins prevent the clearance of amyloid beta from vessel walls. These proteins act by activating a third protein that regulates gene expression and is known to prevent the expression of the lipoprotein receptor protein 1, a factor that promotes clearance of amyloid beta in blood vessel cells.